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. 2019 Jul 24;145(9):2241–2250. doi: 10.1007/s00432-019-02981-5

Fig. 1.

Fig. 1

Characterization of TRIM16 skin-specific knockout mice. a Design of the floxed TRIM16 mouse model, indicating the LoxP sites (orange) flanking Exon 1–6 of the mouse TRIM16 gene. Deleted and retained regions are shown after Cre deletion. b Targeted disruption of the TRIM16 gene, is confirmed by PCR for TRIM16 genomic DNA and mRNA, and immunoblot for mouse TRIM16 protein of keratinocyte primary culture from TRIM16 wild-type (TRIM16+/+), TRIM16 heterozygous (TRIM16+/flox) and TRIM16 homozygous (TRIM16flox/flox) mice. c Densitometry quantification of TRIM16 mRNA and protein expression in keratinocyte cultures from wild-type, heterozygous, and homozygous mice. d TRIM16 keratinocytes-specific knockout mice TRIM16+/+ wild-type, TRIM16+/flox heterozygous and TRIM16flox/flox homozygous mice (N = 9/genotype) were monitored for food consumption/mouse for 5 weeks. Two-way ANOVA was performed to determine statistical significance